Left Ventricular Pressure

What is Left Ventricular Pressure?

The pressure generated in the ventricular chambers of the heart can be measured and used in a variety of ways to understand changes in cardiac function.  Left ventricular pressure (LVP) in conjunction with ventricular volume measurements has a long history of being used to characterize the pressure-volume relationship in the beating heart.

Why Measure Left Ventricular Pressure?

LVP is studied to ensure drugs developed do not negatively alter cardiac contractility.  Increasing or decreasing cardiac contractility is an undesirable property of drugs being developed for non-cardiovascular indications.  The International Conference on Harmonization (ICH) Topic S7A and S7B guidelines only require the assessment of heart rate, blood pressure and the electrocardiogram in nonclinical in vivo safety pharmacology studies.  Assessment of drug effects on contractility is only suggested as an optional follow-up study.  However, early implementation of a measure of cardiac function can greatly reduce the risk of discovering alterations in cardiac performance in late stage drug development

Left ventricular dP/dt is the first derivative of LVP, which is computed  by software algorithms using calculus.  Its peak value, dP/dtmax, is a common, robust and sensitive indicator of changes in cardiac contractility if experimental parameters such as preload, afterload and heart rate are well controlled.  In order to ensure accuracy and avoid errors in the measurement of contractility in experimental animals, the frequency response of the pressure sensing system and the sample rate of the data acquisition system must be optimized for the signal. 

Cardiac contractility is an intrinsic property of heart muscle that affects the heart's performance and can be modified by the autonomic system, circulating hormones, drugs and disease.  Evaluation of a drug's effects on contractility is important in safety assessment studies since either an increase or a decrease may be harmful under certain clinical situations.  An increase in contractility dramatically increases the heart's energy consumption, which translates to increased oxygen consumption and increased coronary blood flow.  This can have serious consequences in the presence of heart disease and/or coronary insufficiency.  A decrease in contractility in an already diseased heart can exacerbate the symptoms and consequences of clinical heart failure.  

How is Left Ventricular Pressure Measured?

In order to accurately measure LVP dP/dtmax, the LVP measurement system must have a high signal to noise ratio and have adequate frequency response to faithfully acquire and store the important information in the signal.  Evidence proves that all important information in those signals occurs at frequencies below 100 Hz.  Therefore, the frequency response of the pressure measurement system must be at least 100 Hz.  

For dogs, nonhuman primates, and normotensive rats, all important information in a LVP signal can be captured with a system with a frequency of 100 Hz.  Although systems with much higher frequency response can be used to measure LVP, the output of these devices must be filtered to allow no frequencies to be acquired that are higher than one-half the sample rate of the acquisition system.  Stated conversely, the sample rate of the acquisition system must be at least 2X the highest frequency contained in the signal.  Failure to follow these principals can lead to incorrect results due to measurement artifacts from high frequency noise, which could be present but not detectable by the investigator.     

Parameters Most Commonly Measured with LVP

  • LVP
  • Diastolic Pressure
  • Heart Rate (HR)
  • Minimum Pressure
  • Peak Systolic Pressure (Sys)
  • LVP and End-Diastolic Pressure (LVEDP)
  • dP/dtmax (+dP/dt)
  • dP/dtmin (-dP/dt)


DSI provides researchers with solutions to measure LVP in conscious, unrestrained subjects using telemetry, or in anesthetized models through hardwired approaches. All data can be collected with Ponemah, our complete physiologic data acquisition and analysis software platform used by physiologists, pharmacologists, and toxicologists to confidently collect, accurately analyze, and quickly summarize study data.

Learn more about Ponemah software from DSI.

Ponemah software, PNM

LVP can be measured in small animals using a dual-pressure PhysioTelTM HD 
implant. DSI's HD-S11, HD-S21 or HD-S20 implants are ideal for high-fidelity applications. The L21 implant, part of DSI's PhysioTelTM Digital product line, allows for LVP data collection in large animals.

Short durations of functional endpoints are collected non-invasively from chemically or physically restrained animals that are connected to external  devices capable of monitoring LVP directly into the Ponemah acquisition and analysis computer system.

234 Left Ventricular Pressure articles citing DSI in Google Scholar




Sarazan, R. D., Kroehle, J., Main, B. (2012):  Left Ventricular Pressure, contractility, and dP/dt max in nonclinical drug safety assessment studies.  Journal of Pharmacological and Toxicology Methods.

Sarazan, R. D., Mittelstadt, S., Guth, B., Koerner, J., Zhang, J., & Pettit, S. (2011). Cardiovascular function in nonclinical drug safety assessment: Current issues and opportunities.  International Journal of Toxicology, 30(3), 272–286.

Bricker, G.G. Adams, S.T. Main, B.W. A Novel method for chronic measurement and assessment of contractility and heart rate in conscious rats by telemetry.

Clark, JE. Kottam, A. Motterlini, R. Marber, MS. Measuring left ventricular function in the normal, infarcted and CORM-3-preconditioned mouse heart using complex admittance-derived pressure volume loops.

Doucette, JW. Goto, M. Flynn, AE. Austin, RE. Husseini, WK. Hoffman, JIE. Effects of cardiac contraction and cavity pressure on myocardial blood flow.

Gizzi. J. O'Donohue, K. Grenwis, J. Yoder, J. Bogie, H. Baird, TJ. Validation of a fully implantable small animal infusion model involving multi-pressure data collection.

Guild, S. Lim, M. Pauly, B. McCormick, D. Kirton, R. Budgett, D. Kondo, M. Stehlin, E. Barrett, C. Malpas, S. Left ventricular pressure measurement in conscious small animals via a novel solid state telemetry pressure sensor.

Guth, B Mittelstadt, S. Rossman,E Pierson, J  Pettit, S Berridge, B Sarazan, D. HESI Cardiac Safety Committee: Prospective Studies to Evaluate the Sensitivity of Animal Models to Predict Effects of Human Drugs on Cardiac Contractility.

Jason, A., Segreti. Andrew, R., Lisowski. James, S., Polakowski. Eric, A., Blomme. Bryan, F., Cox. Andrew, J., King. Simultaneous measurement of arterial and left ventricular pressure in conscious freely moving rats by telemetry.

Main, BW. Strnat, CA. Sarazan, RD. Addition of left ventricular pressure telemetry in dogs and monkeys is a powerful tool in safety pharmacology.

Markert, M. Shen, R. Trautmann, T. Guth, B. Heart rate correction models to detect QT interval prolongation in novel pharmaceutical development. 

Markert, M. Stubhan, M. Mayer, K. Trautmann, T. Klumpp, A. Schuler-Metz, A. Schumacher, K. Guth, B. Validation of the normal, freely moving Gottingen minipig for pharmacological safety testing.

Moors. J. Philp. K, Harmer. A. Lain?e. P, &, Valentin. JP. Incidence of cardiac contractility issues in safety pharmacology studies: is the core battery sufficient?

Norton, K. Iacono, G. Vezina, M. Assessment of the pharmacological effects of inotropic drugs on left ventricular pressure and contractility: An evaluation of the QA interval as an indirect indicator of cardiac inotropism.

Philp. KL. Bowes. J. Harmer. A. Borland. S. Pollard. C. Lainee. P. Valentin. JP. Cardiac contractility strategy: a case study using early preclinical models.

Prior. H. Lainee. P. El-Amrani. F. Martel. E. Richard. S. Wyckmans. M. and, Valentin. JP. Correlation between ejection fraction and dp/dt+ in conscious telemetered dogs dosed with atenolol.

Sweitzer, NK. Use on an implantable left ventricular pressure monitor to detect onset of heart failure.

Van, Vliet, BN. Hu, L. Scott, T. Chafe, L. Montani, JP. Cardiac hypertrophy and telemetered blood pressure 6 wk after baroeceptor denervation in normotensive rats.

VanMiddlesworth. J. O'Donohue. K. Baird. T. Denissen. M. Rindfield. T. Tandem LVP and AoP in a Rat.